Cardiac hypertrophy at autopsy

Abstract

Since cardiac hypertrophy may be considered a cause of death at autopsy, its assessment requires a uniform approach. Common terminology and methodology to measure the heart weight, size, and thickness as well as a systematic use of cut off values for normality by age, gender, and body weight and height are needed. For these reasons, recommendations have been written on behalf of the Association for European Cardiovascular Pathology. The diagnostic work up implies the search for pressure and volume overload conditions, compensatory hypertrophy, storage and infiltrative disorders, and cardiomyopathies. Although some gross morphologic features can point to a specific diagnosis, systematic histologic analysis, followed by possible immunostaining and transmission electron microscopy, is essential for a final diagnosis. If the autopsy is carried out in a general or forensic pathology service without expertise in cardiovascular pathology, the entire heart (or pictures) together with mapped histologic slides should be sent for a second opinion to a pathologist with such an expertise. Indication for postmortem genetic testing should be integrated into the multidisciplinary management of sudden cardiac death.

Proteomic mapping of atrial and ventricular heart tissue in patients with aortic valve stenosis

“…Cardiac fibrosis and enhanced deposition of ECM are signs for decompensation in hypertrophy 4 , 32 , 34 . Indicating a high incidence of fibrosis in diseased tissue, we found fibrosis related proteins (APP, FKBP10, HSPB6 and APCS).…”

Letrozole Accelerates Metabolic Remodeling through Activation of Glycolysis in Cardiomyocytes: A Role beyond Hormone Regulation

“…The nuclei of LV cardiomyocytes were flatter in LTZ-rats than in Veh-rats, and the cytoplasm-to-nucleus ratio occupied the same area in LTZ-rats, compared to Veh-rats (86%, p < 0.05) ( Figure 2 A). As the above histological characteristics pertain to hypertrophic cardiomyopathy [ 31 ], we examined the expression levels of heart failure markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Interestingly, the expression levels of both ANP and BNP were significantly higher in LTZ-rats than in Veh-rats (ANP, 4.92-fold, p < 0.05) (BNP, 2.26-fold, p < 0.05) ( Figure 2 B).…”

“…Next, we examined whether letrozole induced cardiac structural remodeling. It is interesting to note that cardiomyocytes within the LV had a higher cytoplasm-to-nucleus ratio and flatter nuclei in LTZ-rats compared to those in the Veh-rats, an observation that indicates structural remodeling [ 31 ]. Moreover, this histological observation was supported by increased expression levels of heart failure markers [ 38 ], such as ANP and BNP, and physio-functional markers, such as Atp2a2 , Myh6 , and Myh7 , which indicate contractility [ 39 ], cardiomyocyte size [ 40 ] and LV wall thickness [ 41 ], respectively.…”

Symptoms and ECG changes precede sudden cardiac death in hypertrophic cardiomyopathy—A nationwide study among the young in Sweden

“…A total of 38 individuals fulfilled the definitions of HCM, based on medical records and clinical and forensic autopsy, were included in this study. In 2021, the Association for European Cardiovascular Pathology released guidelines for the routine autopsy practice in the post-mortem investigation of cardiac hypertrophy at autopsy [ 23 ]. At the time of this study, no such consensus guidelines were established.…”